Ethylene glycol toxicity

Summary

AGMA with osmolar gap, hypocalcemia, AKI, hematuria, and obstruction
Osmolar gap becomes anion gap as metabolism progresses

Pathophysiology

graph TD
eg["Ethylene glycol"] --> |Alcohol dehydrogenase|glycerald
glycerald["Glyceraldehyde"] --> |Aldehyde dehydrogenase|glycolate
glycolate["Glycolate"] --> glycox
glycox["Glycoxylate"] --> |Thiamine & pyridoxine|metabs["Less toxic metabolites"]
glycox --> oxalate
oxalate["Oxalate"] --> |Calcium|caox
caox["Calcium oxalate"]

Glycolate causes renal tubular damage and oxalate crystal cause urinary obstruction
Hypocalcemia secondary to calcium oxalate formation

Sources

Antifreeze
Windshield fluid
Cleaners
Fuels
Moonshine

Clinical Manifestations

Decreased LOC
Hematuria with flank pain and oliguria
Hypocalcemia
- Cranial nerve palsies
Coma, seizures, tachypnea, and hypotension in late stage

Investigations

Anion gap metabolic acidosis with osmolar gap
- As metabolism progresses the initial osmolar gap is replaced by an anion gap
Order acetaminophen and salicylate levels as well
Lactate can be elevated, either because of lactate or because of false-positive from the ethylene glycol
Monitor renal function, including electrolytes, extended lytes (calcium), and creatinine
Urine microscopy for calcium oxalate crystals, which show up as needle-shaped crystals
Monitor ECG for QTc prolongation from hypocalcemia

Management

ABCs
NG aspiration if within 60 minutes
Sodium bicarb if pH <7.3, with infusion to target pH ≥ 7.35
Thiamine and pyridoxine to shunt glycoxylate metabolism toward less harmful metabolites
Fomepizole or ethanol, which competitively inhibit alcohol dehydrogenase
- Serum ethylene glycol >3.2 mmol/L, or
- Documented toxic ingestion and an osmolar gap > 10, or
- Suspected toxic ingestion and 2 of:
  - pH < 7.3
  - Bicarb < 20
  - Gap (which one?) > 10
  - Urinary oxalate crystals
Hemodialysis if ongoing acidosis and evidence of end-organ damage